Abstract
The aim of this study was to determine the anti-osteoarthritic effects of LI73014F2, which consists of Terminalia chebula fruit, Curcuma longa rhizome, and Boswellia serrata gum resin in a 2:1:2 ratio, in the monosodium iodoacetate (MIA)-induced osteoarthritis (OA) rat model. LI73014F2 was orally administered once per day for three weeks. Weight-bearing distribution and arthritis index (AI) were measured once per week to confirm the OA symptoms. Synovial membrane, proteoglycan layer, and cartilage damage were investigated by histological examination, while synovial fluid interleukin-1β level was analyzed using a commercial kit. Levels of pro-inflammatory mediators/cytokines and matrix metalloproteinases (MMPs) in the cartilage tissues were investigated to confirm the anti-osteoarthritic effects of LI73014F2. LI73014F2 significantly inhibited the MIA-induced increase in OA symptoms, synovial fluid cytokine, cartilage damage, and expression levels of pro-inflammatory mediators/cytokines and MMPs in the articular cartilage. These results suggest that LI73014F2 exerts anti-osteoarthritic effects by regulating inflammatory cytokines and MMPs in MIA-induced OA rats.
Highlights
Osteoarthritis (OA) is a common joint disorder that is characterized by chronic pain, joint inflammation, swelling, and movement limitation [1,2]
Gallic acid is a phytochemical marker for T. chebula fruit raw material, while total curcuminoids and acetyl-11-keto-β-boswellic acid (AKBA) are unique phytochemical markers for C. longa rhizome and B. serrata resin raw materials, respectively
Osteoarthritis (OA) is a painful and debilitating disease characterized by progressive loss of Osteoarthritis (OA) is a painful and debilitating disease characterized by progressive loss of articular cartilage and mild inflammation of the tissue around the joint
Summary
Osteoarthritis (OA) is a common joint disorder that is characterized by chronic pain, joint inflammation, swelling, and movement limitation [1,2]. OA is the most common form of arthritis, which causes tremendous economic burden and disrupts the quality of life. It can be worsened by genetic factors, an overweight status, and post-traumatic arthritis [3]. Medicines or functional foods have generally been used to treat OA; pharmacological treatments of OA are limited in their effectiveness. Management of the condition typically focuses on reducing pain and inflammation using non-steroidal anti-inflammatory drugs (NSAIDs), including acetaminophen, ibuprofen, naproxen, and indomethacin [5]. The efficacy of functional foods such as glucosamine and chondroitin sulfate remain insufficient [4,5]
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